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24 Cards in this Set
- Front
- Back
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what's a urinary symptom characteristic of all diabetics, regardless of subtype?
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increased urine output.
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what is the difference between diabetes mellitus, diabetes insipitus, and brittle diabetes?
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mellitus = abrogated insulin function (either not enough or insensitivity or both). involved upped blood glucose. have high thirst, hunger, glucosuria...
insipitus: all about weird ADH business. destruction of the posterior pituitary cells that release ADH, so have trouble reabsorbing water from the urine and end up with high urine output (remember, all diabetics have high urine output). can also result from insensitivity of kidney to ADH. brittle - totally uncontrolled type 1, with massive swings from hyper to hypo glycemia. |
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in mMol, what's a fasting glucose that indicates diabetes?
what about failing an OGTT in mM? |
7 mMol = 126 mg/dL
11 mMol = 200 mg/dL = failing an OGTT |
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what are the major divisions of diabetes milletus?
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1. Idiopathic: includes type 1 and type 2. note that type 2 rarely includes DKA.
2. Secondary. Includes MODY (mature onset type of young, caused by mutations). also includes gestational, pancreatic disease, drugs, endocrine diesease, antibodies that target insulin receptors, also includes genetic diseases that have diabetes with the (downs, MD, huntington's, cockayne). |
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what percent of US population has diabetes? what percentage of that is type 1?
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8% have diabetes.
5-10% of those are type 1. |
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type 1 - what kinds of antibodies are found, and how common are they?
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>90% have ICCA (islet cell cytoplasmic antibodies)
>80% have ICSA (islet cell surface antibodies) note that both of these decline over time. Also, >80% have antibodies against GAD (glutamic acid decarboxylase) |
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type 1 - what's up with glucagon, and what's the result? how can this be treated?
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lack of insulin prevents glucagon repression - so have lots of it, even when you don't need it.
this can directly lead to ketoacidosis from the breakdown of FA's. can be treated with SOMATOSTATIN - but the problem here is that it stops glucagon pretty seriously. if you're ever hypoglycemic, can't mobilize glycogen and = death. so, can be a bad drug. |
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what happens with glycogen storage in type 1 diabetics?
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think of diabetics as always being in the starvation state - with all that glucagon floating around, they've digested their glycogen stores long ago and have trouble replacing it.
so, generally, they don't have a lot of glucagon stored. |
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how is liver intake of glucose affected in type 1?
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hepatic glucokinase activity (turning glucose into G-6-P) is dependent on insulin, so glucose tends not to absorb into the liver either...it just falls right back out after crossing in through Glut 2.
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what happens to proteins in type 1's?
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proteins get continually degraded for gluconeogenesis.
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where does ketoacidosis come from? what diagnoses it? what does glycerol make you think of? what else does what glycerol does?
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lack of insulin and lots of glucagon stimulates the release of free fatty acids, which are imported to the mitochondria and undergo beta-oxidation.
the excess acetyl CoA produced favors the production of ketone bodies for release. the body thinks its staving and that the brain needs them. an anion gap >12 = acidosis. if also lots of ketones around, know it's ketoacidosis. the extra glycerol that came off the FA's can be used for gluconeogenesis. also, alanine can be used for gluconeognesis. |
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what's the specific diagnostic criteria for DKA?
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pH < 7.3
glucose > 250 bicarb <15 |
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type 2 betus - what's common with insulin production levels over time?
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may increase to deal with insensitivity, but eventually drop off significantly.
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what are some warning signs of type II? thinking waist size, ethnicitiy...
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>40 inches waist men, >35 women.
family history over weight > 25 BMI previous gestational diabetes previous polycystic ovarian syndrome. ethnicity (pacific islander/native american, african) |
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what's a common disease seen in type II, not seen in type 1?
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HHNS
hyperosmolar hyperglycemic nonketonic syndrome. usually type II + incident (volume loss, infection, etc), found in elderly. lots of extra glucose = pee more out = dehydrated = seizures/death. |
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what's a warning sign of HHNS?
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>600 glucose, extreme thirst, no sweating.
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gestational diabetes - how common is it, what's up, what can it lead to? are there risks to baby? what about future pregnancies? treatment?
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placental hormones may make mom insensitive to insulin = up blood glucose.
happens late in pregnancy and DOES NOT CAUSE BIRTH DEFECTS. can make a fat baby - extra glucose crosses into baby, baby ups its insulin and stores lots of extra glucse as fat. fat babies have more trauma during birth (shoulder breakage). also have higher risk of getting the betus later in life. 2/3 chance it'll come back in later pregnancies. treatment is food intake/monitoring/exercise, insulin if needed. |
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heart disease/stroke and betus - what's up with risk? how?
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2-4X higher risk in both heart disease and stroke in betus folks.
glycation can mess with LDL's and cause their half lives to be higher, causing atherosclerosis. also, break endothelial ability to dilate = high BP, up clot formation... |
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dialiysis - what % are diabetics? what % of diabetics will have kidney disease?
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half of dialysis patients are diabetics,
5% of diabetics will develop kidney disease. |
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how does diabetes cause kidney disease?
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high osmotic load means that GFR/RPF have to be increased chronically.
this can lead to a thickening of the basement membrane and gradual closing off of the afferent and efferent arterioles and the capillaries. this drops filtration dramatically. Kimmlesteil-Wilson nodules are capillaries that have been shut by thickening, gradually take over glomeruli. gradually, lack of glomerui raise BUN/urea |
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diabetic kidney damage - how can you tell when it's reversable or permanent?
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when you detect protinuria, game's over.
microalbumunuria = still reversible. |
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cataracts and glaucoma - what causes these?
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cataracts from sorbitol osmotic pressure and swelling.
glaucoma from swelling and pressure sufficient to crush the optic nerve. |
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neuropathy in diabetes - what causes it? what's related?
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caused by "hyperglycemic hypoxia," not sure how that happens. something about bad nerve conduction.
foot disease considered a result of neuropathy (can happen even if blood supply is good). |
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what's ottis externa? what about dry skin?
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fungal ear infection - fungus likes the high glucose/moist environment of the ear and goes to town. can be diagnostic of diabetes.
diabetics get dry skin from lack of sweating (maybe from being dehydrated)? |
